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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.
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PMID:An outbreak of acute methyl alcohol intoxication. 28 45

The effects of alcohol on the central nervous system can be subdivided into three main categories: the effects of acute intoxication (drunkenness, acute encephalopathy, stroke), the effects of tolerance and ethanol withdrawal (delirium tremens, seizures) and the delayed manifestations of chronic alcohol consumption (cerebellar degeneration, Wernicke's encephalopathy, dementia).
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PMID:[Main involvement of the central nervous system in alcoholism]. 141 Sep 80

Male Wistar rats were subjected to repeated weekly episodes of 2 days severe alcohol intoxication (intragastric intubation) and 5 days of withdrawal. In half of the animals the withdrawal reaction was attenuated during the first nine weekly episodes by intragastric intubations with phenobarbital. During episodes 10-14 both phenobarbital treated and phenobarbital untreated animals were allowed to develop a withdrawal reaction; all animals were video-recorded during withdrawal and the records were rated blindly for the occurrence of convulsive seizures. The results were analyzed by step-wise logistic analysis of regression including phenobarbital treatment, alcohol dose and intoxication score as explanatory variables for the occurrence of convulsive seizures. The animals that had been in withdrawal during all episodes developed significantly more convulsive seizures compared with animals that had their first nine withdrawal episodes attenuated by phenobarbital. The development of withdrawal seizures depended on repeated episodes of withdrawal, whereas repeated alcohol intoxication per se did not explain the development of seizures. There were no differences between the groups in the severity of the non-convulsive signs of alcohol withdrawal. Thus the development of seizures and the non-convulsive signs of alcohol withdrawal may result from two pathogenetically different mechanisms: 1) seizures from a cumulative kindling-like effect over long time periods and 2) physical signs of alcohol withdrawal may reflect the degree of physical dependence during the most recent drinking bout.
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PMID:Convulsive behaviour during alcohol dependence: discrimination between the role of intoxication and withdrawal. 158 67

We reported a 39-year-old man with punch drunk syndrome who had cerebellar ataxia, seizure and dementia. CT scan of the brain revealed remarkable atrophy and enlargement of the ventricular system. MRI of the brain showed severe atrophy which was especially evident in the frontal base. On RI cisternography both early ventricular reflux at 3 hours and delayed ventricular stasis at 52 hours were found, which resembled the findings of the normal pressure hydrocephalus. The MRI and RI cisternographic findings suggested that the remarkable brain atrophy and enlargement of the ventricular system were caused by repeated KARATE traumas including minor brain contusion or subarachnoid hemorrhage in the base of the brain, since traumatic brain contusions affect particularly the orbital surfaces of the frontal lobes and the lateral and inferior surfaces of the temporal lobes. Communicating hydrocephalus may be one of the pathogenesis of punch drunk syndrome.
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PMID:[Punch drunk syndrome due to repeated karate kicks and punches]. 208 30

The results presented here strongly suggest that quantitative electroencephalography and event-related potentials are excellent research tools and may be clinically useful as non-invasive monitors of psychotropic drug action and encephalopathies. Our initial data with acute mild alcohol intoxication show that acute tolerance may be reflected in qEEG but not in P3 latency. Since predictably some brain functions may show tolerance, and others not, these approaches may be useful probes. The amplitude of N1-P2 appears to differentiate alcoholics with and without a history of withdrawal seizures. This technique may thus prove useful in determining treatment and monitoring treatment effects in alcohol withdrawal. P3 latency appears to be normal in Korsakoff's syndrome, unlike in Alzheimer's disease. The combination of the event-related potentials with neuropsychology and magnetic resonance imaging scans should be invaluable for future research in these patient groups. Many patients with severe liver disease superficially appear mentally intact. The event-related potential and quantitative electroencephalography findings we have demonstrated may indicate those at greater risk for alterations in brain functioning. These techniques may also prove useful in diagnosing other "subclinical" encephalopathies and further our understanding of the underlying brain pathophysiology.
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PMID:Acute, withdrawal, and chronic alcohol effects in man: event-related potential and quantitative EEG techniques. 229 41

During the past century, infrequent, anecdotal reports of sleep-related violence with forensic science implications have appeared. Recent rapid developments in the field of sleep-disorders medicine have resulted in greater understanding of a variety of sleep-related behaviors, and formal sleep-behavior monitoring techniques have permitted their documentation and classification. Sleep-related violence can be associated with a number of diagnosable and treatable sleep disorders, including (1) night terrors/sleepwalking, (2) nocturnal seizures, (3) rapid eye movement (REM) sleep-behavior disorder, (4) sleep drunkenness, and (5) psychogenic dissociative states occurring during the sleep period. Potentially violent automatized behavior, without consciousness, can and does occur during sleep. The violence resulting from these disorders may be misinterpreted as purposeful suicide, assault, or even homicide. Sleep-related violence must be added to the list of automatisms. A classification system of both waking and sleep-related automatic behavior is proposed, with recommendations for assessment of such behavior.
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PMID:Sleep violence--forensic science implications: polygraphic and video documentation. 232 33

One hundred patients undergoing treatment for alcohol-related problems in Kuwait's only psychiatric hospital were studied. Eighty-three Kuwaitis and 17 non-Kuwaitis (78 inpatients and 22 outpatients) were compared on two variables, i.e. nationality and drinking category. Kuwaiti patients were more likely to be violent while drunk and to receive benzodiazepine prescriptions while non-Kuwaiti patients were better educated and suffered more alcohol withdrawal seizures. Heavy drinkers were prescribed more benzodiazepines. Light drinkers were involved in more road accidents and were more likely to be prescribed major tranquillizers. The relationship between benzodiazepines use and alcohol withdrawal symptoms is discussed and its implications in patient care in Kuwait are stressed.
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PMID:Some clinical and behavioural aspects of patients with alcohol dependence problems in Kuwait psychiatric hospital. 286 26

Clinically, patients with Delirium Tremens (DT) and acute alcohol hallucinosis (impending DT) appear excited with vivid false perception. Cerebral blood flow and eeg correspondingly point to hyperexcitability in the CNS during these conditions. Clinical trials with barbital treatment in alcohol withdrawal shows that the amount of drug and the drug plasma concentration is the same no matter whether the physical signs of withdrawal are accompanied by hallucinations and clouding of consciousness. The psychotic signs in DT and acute alcoholic hallucinosis develops after many years of alcoholism as does seizures. We hypothesize that physical withdrawal is determined by the degree of physical dependence developed during the most recent drinking period whereas the psychotic signs and seizures are due to a cumulated CNS hyperactivity developed over many years of repeated alcohol intoxication and withdrawal. Changes of electrolyte concentrations in plasma or CSF do not play an important role in the pathogenesis of DT and related clinical states except that changes in calcium and inorganic phosphate metabolism indirectly point to changes in membrane excitability. A new model for a study of rapidly repeated intoxication and withdrawal episodes in rats has shown that repetition of episodes augments the convulsive component of withdrawal whereas the non-convulsive signs are dependent on the most recent episode only. The augmentation of the convulsive component correlates with regional differences in brain glucose consumption. Furthermore, synaptic proteins and acidic phospholipids may be involved in the development of CNS hyperexcitability during alcohol withdrawal. In conclusion both clinical and experimental studies indicate that severe alcohol withdrawal reactions may consist of two components: 1) Physical withdrawal signs determined by recent physical dependence. 2) A long term cumulated CNS hyperexcitability relating to seizures and psychotic signs during withdrawal. This state is elicited by alcohol withdrawal but it represents a cumulated and permanent or long lasting CNS dysfunction in alcoholics. The precise biochemical/pathophysiological mechanisms for the development of the two-component dysfunction still remain to be clarified in detail.
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PMID:Delirium tremens and related clinical states: psychopathology, cerebral pathophysiology and psychochemistry: a two-component hypothesis concerning etiology and pathogenesis. 306 44

Approximately 25% of patients with epilepsy will have their first seizure after the age of 25 years. These individuals will need special attention with regard to etiology. Brain tumor is one of several causes that may be suspected. The present study of 221 patients with late-onset epilepsy from the University Clinic of Neurology, Hvidovre Hospital, Copenhagen, Denmark, was undertaken to look for means to select those cases in which computerized tomography (CT) scan should be performed. Brain tumor was the cause in 16% and cerebrovascular infarctions in 14%. The major etiological group was the one in which no cause could be detected (38%). Alcohol abuse as the etiology--defined as cases with a history of long-standing alcohol overuse, concomitant signs of alcohol intoxication, and spontaneous recurrent epileptic seizures--made up a group of one-fourth of all the patients with late-onset epilepsy. Comparison of the history, clinical symptoms and signs, EEG abnormalities, and CT scan speaks in favor of some consideration being given to the first three parameters before the CT scan is performed.
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PMID:Late-onset epilepsy: etiologies, types of seizure, and value of clinical investigation, EEG, and computerized tomography scan. 400 82

Drinking habits of 156 consecutive polyneuropathic and 106 consecutive pressure palsy patients were evaluated in retrospect. Respectively, 46 patients (30%) had alcohol polyneuropathy and 32 (30%) got pressure neuropathy while being drunk and these patients were analyzed in more detail. Most of the patients with alcoholic neuropathies were men, those with polyneuropathy being older than those having pressure palsies. Pressure neuropathy coincided with alcoholic polyneuropathy in 13 patients (28%). Other medical complication of heavy alcohol drinking (i.e. liver diseases, seizures and cerebellar signs) were seen in 54% of the patients with polyneuropathy and in 6% of the patients with pressure palsies. Heavy drinking prolonged the disability due to pressure palsy. The present study confirms the significant role of alcohol abuse in etiology of peripheral neuropathies. Heavy drinking seems to worsen the prognosis of these neuropathies.
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PMID:Drinking habits and peripheral alcoholic neuropathy. 627 9


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